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H pylori may trigger cancers by switching off a tumour suppressor

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Silencing of a cell surface adhesin in gastric mucosa in Helicobacter pylori infection may lead to gastric cancer, a molecular study has suggested. Methylation of the E-cadherin gene promoter—which inactivates its normal tumour suppressor function—was evident in gastric mucosa and significantly associated with H pylori infection in patients with chronic gastritis. It was absent from normal gastric mucosa but evident in 57% (12/21) of intestinal metaplasias, 58% (15/26) of primary gastric cancers, and 65% (21/32) of metastatic lymph node cancers. Methylation was congruent for 92% (11/12) intestinal metaplasias and primary cancers and 85% (17/20) primary and secondary metastatic cancers from the same patients.

Weaker immunostaining for E-cadherin—indicating methylation—occurred in most (11/13) primary cancers tested and most (7/9) metastatic cancers Methylation was significantly linked to depth of tumour invasion and spread. It was not related to H pylori infection here, however. The authors propose that H pylori infection of gastric mucosa triggers E-cadherin methylation and may set the scene for intestinal metaplasia and invasive cancer.

Gastric mucosa were obtained from 35 patients with dyspepsia but no metaplasia or dysplasia during endoscopy and surgical resection specimens from patients with sporadic gastric cancers. E-cadherin methylation was determined by specific PCR.

E-cadherin is a membrane protein involved in cell adhesion and in its native state an important tumour suppressor. H pylori infection has been implicated in the development of gastric cancer. The study set out to examine the association between E-cadherin gene methylation and H pylori infection in gastric cancer.

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